Uric acid is an end product of nitrogen metabolism in the human body (the main product being urea), and is found in small amounts in blood and urine. The disease ‘gout’ in humans is associated with abnormally high levels of uric acid in the blood and in the urinary system and with the formation of uric acid crystals in or near the joints. The symptoms caused by uric acid crystals include redness, swelling, inflammation, pain, kidney stones, and reduced movement. Increased concentration of uric acid in the human blood stream may also result in one form of kidney stones when the uric acid crystallizes into a solid inside the kidney. The uric acid crystals are made of salts of urate anions and cations including ammonium, sodium, potassium, calcium and magnesium. Ammonium urate is a uric acid crystal that often forms stones or uroliths in the urinary system. Sodium urate is a uric acid crystal that often causes symptoms in or near the joints in gout.
Medications such as NSAIDs, corticosteroids and allopurinol are commonly used to treat gout. These medications are effective, but have significant adverse side-effects. None of these medications are known to be mixed together into a single medicament.
Since the 1800s, colchicine has been a standard treatment for acute gout. Colchicine facilitates the elimination of uric acid from the body. While colchicine is effective, it often causes nausea, vomiting and diarrhea. These side-effects are most common when this drug is taken orally, and because of their unpleasant nature, non-steroidal anti-inflammatory drugs (NSAIDs) have become the treatment of choice for most acute attacks of gout. The NSAID that is most widely used to treat acute gout is indomethacin. NSAIDs also have significant toxicity, but if used for the short-term, are generally well-tolerated.
Therapy directed at normalizing uric acid levels in the blood may be considered for patients who have had multiple gout attacks or who have developed tophi or kidney stones. Several drugs that help the kidneys eliminate uric acid are available, such as probenecid, and a drug that blocks production of uric acid by the body, such as allopurinol. The choice between these two types of drugs depends on the amount of uric acid in the urine.
What is desired are improved formulations for relieving symptoms associated with uric acid crystals that are simple to administer, effective at reducing symptoms, have reduced toxicity, and are less expensive than formulations and treatments that are currently available. What are also needed are formulations for preventing symptoms associated with uric acid crystals in the body.